Docosahexaenoic Acid Promotes Cd Excretion by Restoring the Abundance of Parabacteroides in Cd-Exposed Mice

Molecules. 2023 May 21;28(10):4217. doi: 10.3390/molecules28104217.

Abstract

As a common harmful pollutant, cadmium (Cd) can easily enter the human body through the food chain, posing a major threat to human health. Gut microbiota play a key role in Cd absorption. Docosahexaenoic acid (DHA) is thought to have a potential role in the treatment of Cd poisoning. This study investigated the therapeutic effect and mechanism of DHA in Cd-exposed mice from the perspective of the gut microbiota. The results showed that DHA significantly increased the Cd content in feces and decreased the Cd accumulation in the organs of mice. The gut microbiota results showed that DHA significantly restored the abundance of Parabacteroides in the gut microbiota of Cd-exposed mice. Parabacteroides distasonis (P. distasonis), a representative strain of the Parabacteroides, also showed Cd- and toxicity-reduction capabilities. P. distasonis significantly restored the gut damage caused by Cd exposure. At the same time, P. distasonis reduced the Cd content in the liver, spleen, lung, kidneys, gut, and blood to varying degrees and significantly increased the Cd content in feces. The succinic acid produced by P. distasonis plays an important role in promoting Cd excretion in Cd-exposed mice. Therefore, these results suggest that P. distasonis may have a potential role in DHA-mediated Cd excretion in Cd-exposed mice.

Keywords: Parabacteroides distasonis; cadmium; cadmium excretion; docosahexaenoic acid; gut microbiota; succinic acid.

MeSH terms

  • Animals
  • Body Fluids*
  • Cadmium / toxicity
  • Docosahexaenoic Acids / pharmacology
  • Feces
  • Gastrointestinal Microbiome*
  • Humans
  • Mice

Substances

  • Cadmium
  • Docosahexaenoic Acids

Grants and funding

This work was supported by the National Natural Science Foundation of China (No. 32172215) and the Natural Science Foundation of Guangdong Province (No. 2019A1515010809 and No. 2021A1515012443).